High-Level Clonal FGFR Amplification and Response to FGFR Inhibition in a Translational Clinical Trial.

@article{Pearson2016HighLevelCF,
  title={High-Level Clonal FGFR Amplification and Response to FGFR Inhibition in a Translational Clinical Trial.},
  author={Alex Pearson and Elizabeth C Smyth and Irina S. Babina and Maria Teresa Herrera-Abreu and Noelia Tarazona and Clare Peckitt and Elaine Kilgour and Neil R. Smith and Catherine Geh and Claire Rooney and Rosalind J. Cutts and James Campbell and Jian Ning and Kerry Fenwick and Amanda Swain and Gina Brown and Sue Chua and Anne L. Thomas and Stephen R. D. Johnston and Mazhar Ajaz and Kate A Sumpter and Angela Gillbanks and David J Watkins and Ian Chau and Sanjay Popat and David Cunningham and Nicholas C. Turner},
  journal={Cancer discovery},
  year={2016},
  volume={6 8},
  pages={
          838-851
        }
}
UNLABELLED FGFR1 and FGFR2 are amplified in many tumor types, yet what determines response to FGFR inhibition in amplified cancers is unknown. In a translational clinical trial, we show that gastric cancers with high-level clonal FGFR2 amplification have a high response rate to the selective FGFR inhibitor AZD4547, whereas cancers with subclonal or low-level amplification did not respond. Using cell lines and patient-derived xenograft models, we show that high-level FGFR2 amplification… 

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